Why does pulmonary disease cause siadh

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We would like to describe the case of a year-old male patient who was taken to the Emergency Department because of diffuse abdominal pain and vomiting, as well as alarming symptoms that included slow mental reactions and disorientation. The patient had a history of chronic obstructive pulmonary disease caused by severe asthma treated chronically with oral corticosteroids, non-insulin-dependent diabetes mellitus, arterial hypertension and a transurethral resection of the bladder because of a neoplasia four years before.

The presence of hypothyroidism and adrenal failure was ruled out. The patient appeared to present SIADH and so water was restricted and hypertonic intravenous saline solution was administered. When searching for the cause of SIADH, a brain MRI scan was carried out but no significant findings were made and a chest CT was performed which showed increased density of alveolar characteristics limited to basal segments of the right upper lobe that was very suggestive of pneumonia figure 1A.

Neurologic disorders in consecutive patients with small cell lung carcinoma. Cancer — Jacob S , Spinler SA. Hyponatremia associated with selective serotonin-reuptake inhibitors in older adults.

Annals of Pharmacotherapy 40 — Citalopram therapy as a risk factor for symptomatic hyponatremia caused by the syndrome of inappropriate secretion of antidiuretic hormone SIADH : a case report.

Pharmacopsychiatry 38 — Incidence of selective serotonin reuptake inhibitor induced hyponatraemia due to the syndrome of inappropriate antidiuretic hormone secretion in the elderly. International Journal of Geriatric Psychiatry 13 — Holden R , Jackson MA. Lancet Journal of Pediatric Endocrinology and Metabolism 13 — Severe hyponatremia and inappropriate antidiuretic hormone secretion following ecstasy use.

Academic Emergency Medicine 5 — The natural history of post-traumatic neurohypohysial dysfunction. European Journal of Endocrinology — Posterior pituitary dysfunction following traumatic brain injury. Journal of Clinical Endocrinology and Metabolism 89 — The osmotic thresholds for thirst and vasopressin release are similar in healthy man. Clinical Science 71 — Vasopressin function in the syndrome of inappropriate antidiuresis.

Annual Review of Medicine 31 — Biosynthesis of vasopressin in vitro and ultrastructure of a bronchogenic cancer. Journal of Clinical Investigation 51 — Atrial natriuretic factor and arginine vasopressin production in tumor cell lines from patients with lung cancer and their relationship to serum sodium. Cancer Research 53 67 — American Journal of Physiology.

Endocrinology and Metabolism E — E Neurogenic disorders of osmoregulation. American Journal of Medicine 72 — Baylis PH. The syndrome of inappropriate antidiuretic hormone secretion.

International Journal of Biochemistry and Cell Biology 35 — Nephrogenic syndrome of inappropriate antidiuresis. Nephrogenic syndrome of inappropriate antidiuresis in adults: high phenotypic variability in men and women from a large pedigree. Journal of the American Society of Nephrology 18 — Studies of renal aquaporin-2 expression during renal escape from vasopressin-induced antidiuresis. Advances in Experimental Medicine and Biology — Changes in urine concentration during prolonged administration of vasopressin and water.

American Journal of Physiology — Pathological role of aquaporin-2 in impaired water excretion and hyponatremia. Journal of Neuroendocrinology 16 — Role of renal aquaporins in escape from vasopressin-induced antidiuresis in rat. Journal of Clinical Investigation 99 — Vasopressin V2 receptor binding is down-regulated during renal escape from vasopressin-induced antidiuresis. Endocrinology — Escape from vasopressin-induced antidiuresis: role of vasopressin resistance of the collecting duct.

American Journal of Physiology F — F Verbalis JG. Adaptation to acute and chronic hyponatremia: implications for symptomatology, diagnosis, and therapy.

Seminars in Nephrology 18 3 — Electrolyte-induced demyelination in rats. Role of the blood—brain barrier and edema. Acta Neuropathologica 88 — Organic osmolytes in acute hyponatremia.

Chronic hyponatremic encephalopathy in postmenopausal women: association of therapies with morbidity and mortality. Journal of the American Medical Association — Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits.

American Journal of Medicine 71e1 — 71e8. Chronic hyponatraemia induces severe bone loss and mild hypogonadism in both male and female rats.

Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Annals of Internal Medicine — This paper forms part of a supplementary issue of European Journal of Endocrinology. Otsuka Pharmaceutical Europe Ltd. Author guidelines Reasons to publish Ethical policy Open-access policy Publication charges Author resource centre. Advanced Search Help.

The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences in European Journal of Endocrinology. Correspondence should be addressed to C J Thompson; Email: christhompson beaumont. The dose was reduced to 7. Course of blood sodium levels during admission. SIADH is characterized by the sustained release of arginine-vasopressin ADH in the absence of the usual stimuli, particularly hyperosmolarity and hypovolemia. Symptoms are non-specific, and can range from nausea, dizziness, general malaise, agitation and confusion to seizure or coma in cases of sudden onset or very low blood sodium levels.

Hyponatremia due to SIADH occurs quite frequently in small cell carcinoma, sometimes as a first manifestation, 9—11 and is associated with decreased survival. When SIADH develops with mild hyponatremia, water restriction and furosemide should be considered, and in patients who are not candidates for these measures or whose clinical symptoms persists, the use of tolvaptan is recommended. We believe that this case of SIADH associated with a COPD exacerbation illustrates the need to include blood sodium monitoring in the management of these patients, in order to detect and reduce the morbidity and mortality of this fluid-electrolyte imbalance.

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This item has received. Article information. Full Text. Pauwels, A. Buist, P. Calverley, C. Jenkins, S. Hurd, GOLD Scientific Committee Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease.. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease.

Am Respir Crit Care Med, , pp. Almagro Mena, M. Med Clin Barc , , pp. Chalela, J. These patients are usually volume depleted and further fluid restriction can be dangerous to the patient.

It should be noted that aldosterone is unaffected in SIADH and the sodium balance will be usually normal. If isotonic saline is administered, the water will be retained and sodium will be excreted in urine, leading to possible worsening of hyponatremia. Hypertonic saline raises serum sodium, but the response will partially dissipate over time. The effect of salt tablets can be enhanced by administration of a loop diuretic like furosemide which interferes with the countercurrent concentrating mechanism by decreasing sodium chloride reabsorption in the thick ascending limb of loop of Henle.

This results in excretion of isotonic urine and considerable fluid loss. The usual dose is 9 g salt daily with 20 mg oral furosemide twice a day. Antidiuretic response is mediated by V2 receptor, while V1a and V1b receptors cause vasoconstriction and adrenocortcotropic hormone ACTH hormone release.

Vasopressin receptor antagonists produce a selective water diuresis without interfering with sodium and potassium excretion. Tolvaptan, satavaptan and lixivaptan are selective V2 receptor antagonists, while conivaptan blocks both V1 and V1a receptors. In a randomized controlled trial, intravenous conivaptan significantly raised serum sodium concentration. The use of V2 receptor antagonists is limited due to increased thirst,[ 35 ] rapid correction of hyponatremia as demonstrated in SALT trials and the high cost.

Vasopressin receptor antagonists should not be used in hyponatremic patients who are volume depleted. It is a tetracycline derivative which induces drug-induced diabetes insipidus by acting on the collecting tubule cell to diminish its responsiveness to ADH. Rapid correction of hyponatremia can lead to central pontine myelinolysis. The risk is highest in premenopausal women.

Osmotic demyelination syndrome ODS occurs with rapid correction of severe hyponatremia. There are several risk factors for ODS which include serum sodium concentration at presentation, duration of hyponatremia and rapid rate of correction, alcoholism, malnutrition, liver disease and hypokalemia.

Clinical features can be delayed by a few days after rapid sodium correction. Symptoms include neurological manifestations like dysarthria, dysphagia, paraparesis, quadriparesis, confusion, coma, etc. Seizures are very rare. Locked-in syndrome can occur when there is bilateral pontine demyelination. ODS can be detected by magnetic resonance imaging MRI scan, but it may take up to 4 weeks to become positive. Hence, a negative study earlier in the course does not rule out ODS.

Treatment is often difficult; importance should be given to prevention. As previously discussed, slow correction of hyponatremia is essential in the prevention of ODS. Minocycline[ 42 , 43 ] has been shown to be efficacious in preventing ODS if concurrently administered with hypertonic saline or if initiated within 24 hours of correction of hyponatremia.

ODS is associated with poor prognosis. Few case reports suggest benefit from early relowering of serum sodium. Supportive treatment to prevent aspiration pneumonia and ventilatory care are needed. Plasmapheresis[ 44 ] may also be beneficial. CSW is a distinct disease which occurs in the setting of CNS disorders which manifest with hyponatremia. It was originally described by Peters et al. However, some authorities argue that such a condition does not exist and CSW is a misnomer.

There are case reports of CSW occurring in the presence of pituitary adenoma[ 47 ] Distinction from SIADH is often difficult, but essential as the treatment is different in both the conditions. Salt tablets can be administered once the patient can tolerate oral medications. It is common to use fludrocortisone, a mineralocorticoid in neurosurgical practice, which is found to be useful in CSW.

Many of the sick, hospitalized patients are on diuretics, and diagnosing SIADH is difficult in these situations. Urine sodium and fractional excretion of sodium FE-Na are of little use in this setting to differentiate between SIADH and hyponatremia due to diuretic use. Wiebke et al. Advancing age itself may be a risk factor for SIADH due to the normal aging process that affects fluid balance.

Normal physiologic changes associated with aging such as elevated ADH and atrial natriuretic hormone levels as well as an increased responsiveness to osmotic stimulation predisposes elderly patients to SIADH. There are several factors associated with the occurrence of hyponatremia in the postoperative period.

Besides, stress, hypotension, pain, general anesthesia and medications used after surgery like opioids may precipitate the development of SIADH.

Hyponatremia is commonly encountered in inpatient settings and rarely encountered in outpatient clinics. SIADH is a common cause of hyponatremia. An active search for the cause of SIADH should be done and offending cause should be treated whenever possible. Treatment is mainly fluid restriction. However, in CNS disorders associated with hyponatremia, CSW should be ruled out, as the treatment modalities are different. ODS is a serious, but rare complication of treatment of hyponatremia.

Sodium correction should be done gradually in chronic hyponatremia. There are several other causes of hyponatremia, including hypothyroidism and hypoadrenalism, and these disorders should be ruled out prior to diagnosing as SIADH. Source of Support: Nil. Conflict of Interest: None declared. National Center for Biotechnology Information , U. Indian J Endocrinol Metab.

Binu P. Praveen V. Author information Copyright and License information Disclaimer. Corresponding Author: Dr. E-mail: ude. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article has been cited by other articles in PMC. Keywords: Hyponatremia, syndrome of inappropriate antidiuretic hormone secretion, cerebral salt wasting.

Drugs A number of drugs can enhance ADH release or action. Open in a separate window. Malignancies Lung tumors, especially small cell carcinoma, produce ADH ectopically. Surgery Major surgical procedures, which include abdominal and thoracic surgeries, can cause hypersecretion of ADH, probably mediated by pain afferents.